May 11, 2026
May 10, 2026
Author(s)Marco Meglio, Rebecca Wilkins
Rebecca Wilkins, Divisional Vice President of R&D Neuromodulation at Abbott, discusses the evolving role of deep brain stimulation in Parkinson disease, including patient selection, newer DBS technologies, and integration with emerging therapies.
As Parkinson disease (PD) progresses, many patients reach a point where medication alone is no longer sufficient to control symptoms such as tremor, rigidity, slowness, and motor fluctuations. For these individuals, deep brain stimulation (DBS) has become an increasingly important treatment option, offering targeted neuromodulation to help improve motor control and reduce the burden associated with escalating medication schedules.
Often described as a “pacemaker for the brain,” DBS works by delivering electrical stimulation to specific brain regions involved in motor circuitry. Over the last several years, the field has continued to evolve through innovations such as directional leads, adaptive programming strategies, and remote care technologies aimed at personalizing therapy and improving long-term patient management. At the same time, clinicians are reassessing the timing of referral for DBS evaluation, particularly as newer infusion therapies and investigational disease-modifying approaches continue to emerge within Parkinson disease care.
During PD Awareness Month (April), NeurologyLive® spoke with Rebecca Wilkins, Divisional Vice President of R&D Neuromodulation at Abbott, about the current state of DBS technology and how the treatment landscape is changing. In the discussion, Wilkins outlined the mechanistic rationale behind DBS, key considerations for patient selection, and the ways newer neuromodulation technologies may influence programming strategies and patient outcomes moving forward.
Can you outline how DBS modulates basal ganglia circuitry and how this translates into improvements in motor symptoms for patients with Parkinson's disease?
Rebecca Wilkins: Deep brain stimulation (DBS) works by delivering precisely timed electrical pulses to specific areas within the brain's basal ganglia circuitry, which are involved in motor control, to help control PDP symptoms.1 DBS systems include two main components that facilitate this process:
- An implantable pulse generator (IPG), a small device placed under the skin of the chest, produces these electrical pulses.
- Thin wires, known as leads, are surgically implanted to deliver these electrical pulses directly to the targeted brain regions. These DBS systems can utilize two different types of batteries: rechargeable and non-rechargeable.
- These electrical outputs function much like a pacemaker for the brain, disrupting abnormal, overactive brain signals to provide significant improvements in motor symptoms for patients with PD, particularly when medication alone is no longer sufficient.
- DBS offers an advantage by reducing the burden of the strict medication schedule often associated with pharmaceutical management, while also providing relief for all the major symptoms of PD. It is particularly beneficial in improving movement symptoms, such as tremor, stiffness, and slowness, especially when these symptoms respond to levodopa.
- It should be noted that tremor itself can improve with DBS even if it has not responded to levodopa.
- Furthermore, DBS effectively addresses medication side effects, including dyskinesia (extra, involuntary movements), either directly or by enabling lower medication doses. This improves "on time" without bothersome dyskinesias and ensures sustained symptom improvement for patients with PD.3
May 4, 2026
Researchers say supplements may have cognitive benefits, call for more studies
Written by Marisa Wexler, MS | May 1, 2026
- Probiotics did not reduce anxiety in Parkinson's patients more than a placebo.
- However, probiotic use showed potential cognitive improvements.
- Further research is needed to confirm probiotics' cognitive benefits in Parkinson's.
A small clinical trial testing whether a probiotic supplement could ease anxiety in people with Parkinson’s disease found that it was no better than a placebo.
However, patients given the supplement showed significant improvements on cognitive tests compared with those given the placebo. The researchers cautioned that this finding should be interpreted cautiously, and called for further studies to explore whether probiotics may help improve cognition in Parkinson’s.
“While no group differences were observed for neuropsychiatric symptoms following the 12-week intervention, the potential cognitive benefits seen in the probiotic group warrant further investigation,” they wrote in the study, “Probiotic supplementation for anxiety symptoms in people with Parkinson’s disease: a randomized, double-blind, placebo-controlled trial,” which was published in npj Parkinson’s Disease.
Anxiety — uncontrollable worry or fear — is a common nonmotor symptom of Parkinson’s that can cause substantial distress. Although talk therapy and medication may help manage anxiety, these available therapies don’t work for everyone. Researchers are actively searching for new ways to help ease anxiety.
Probiotics are a broad class of supplements containing living bacteria that are thought to be beneficial for health. More than 20 clinical trials have tested whether various probiotic supplements can ease anxiety in the general population, with some reporting promising effects. A few studies have also tested whether probiotics can help ease various symptoms of Parkinson’s, but there’s minimal data on whether probiotics may help ease anxiety in people with this neurological disease.
May 1, 2026
By Nicole Gregory, Published on March 16, 2026
From walking and strength training to yoga and balance work, doctors say regular exercise can ease Parkinson’s symptoms and improve quality of life — and it’s now central to care.
In 2023, when Samantha Dunn was 58, she started to notice subtle changes in her body and the way she moved. Her handwriting became smaller and she had a strange twitch in one of her fingers. She also felt her left leg was weaker than her right. When her cousin mentioned he’d been diagnosed with Parkinson’s disease after experiencing similar symptoms, Samantha had a sinking feeling she had it, too.
After finally receiving the diagnosis — her primary care doctor had initially brushed off her symptoms — the neurologist said that exercise was the prescription. “After that, I was assigned to a movement disorder specialist,” Dunn said, “who further elaborated on the amount of exercise recommended — high intensity, five days a week for a half an hour, plus yoga for balance.”
Dunn, who lives in Southern California, now considers herself lucky. Her exercise routine has grown to include vigorous walking and weight lifting, along with horseback riding. If she has to work long hours at her desk, she takes 10-minute breaks to do push ups or use free weights she keeps nearby.
“Exercising makes a huge difference in my energy level,” she said, adding that it also helps with mental clarity that cuts through her occasional brain fog. She credits yoga for helping her with balance.
Improving symptoms and slowing progression
It was patients like Dunn and their physical therapists who, decades ago, were the first to notice the benefits of exercise on symptoms of Parkinson’s, said John Walsh, Ph.D., associate professor of gerontology and associate dean of education at University of Southern California in Los Angeles, whose research is focused on neuroscience and brain diseases such as Parkinson’s.
Research then confirmed those experiences, Walsh said. A 2022 study from Japan published in the journal Neurology tracked 237 people with early Parkinson’s for five years and found that moderate to vigorous exercise were associated with slower decline of their posture and gait stability.
And a 2024 research review published in the Journal of Neurology, Neurosurgery & Psychiatry
Apr 30, 2026
Routine biopsies could reveal neurodegenerative risk
Written by Andrea Lobo | April 29, 2026
- Gut protein misfolding can predict neurodegenerative diseases like Parkinson's years before symptoms appear.
- Routine gut biopsies showing PME were linked to neurological symptom onset nearly seven years later.
- This offers a potential early-detection tool for people at risk, enabling earlier intervention.
Routine gut biopsies may turn up evidence of protein misfolding, predicting the risk of developing neurodegenerative diseases such as Parkinson’s disease years before neurological symptoms appear, a study suggested.
Researchers from the University of Aberdeen, NHS Grampian, and NHS Highland found that more than half of people who had digestive symptoms but no diagnosed neurological disease had a condition called protein misfolding enteropathy (PME). PME predicted disease with greater than 80% sensitivity and was linked to neurologic symptom onset nearly seven years later.
“The study highlights the urgent need for better detection tools for neurodegenerative diseases,” Jenna Gregory, PhD, professor at the University of Aberdeen and lead author of the study, said in a university news story. “Many of these conditions still lack effective treatment options, making early detection and scalable screening approaches especially important for improving patient outcomes.”
The study, “Protein misfolding enteropathy predicts and prognosticates 2 neurodegenerative disease years before symptom onset,” was published in Gastroenterology. It was funded by NHS Grampian Charity, Target ALS, and LifeArc.
Early treatment strategies ‘urgently needed’
Accumulation of misfolded proteins is a common hallmark of neurodegenerative diseases, including Parkinson’s, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS), thought to contribute to the progressive loss of nerve cells. In Parkinson’s, the buildup of toxic clumps of misfolded alpha-synuclein is believed to contribute to the death of nerve cells that produce dopamine, a signaling molecule involved in motor control.
By the time Parkinson’s symptoms appear, substantial nerve cell loss has already occurred, and therapies are usually less effective. “Early intervention strategies aligned with readily accessible targets for biomarker development are urgently needed for these diseases,” the researchers wrote.
The team focused on PME, as gastrointestinal symptoms often precede neurological symptoms in certain neurodegenerative conditions. They retrospectively analyzed gut biopsies from 196 people (53.1% women, median age 70) with unexplained gastrointestinal symptoms, followed for a median of 14 years to track the development of neurodegenerative diseases. The team assessed three key proteins associated with neurodegeneration: alpha-synuclein, TDP-43, and tau.
Apr 29, 2026
Along with neurodegeneration, vascular issues may drive disease progression
- Parkinson's disease involves toxic alpha-synuclein protein clumps damaging both brain cells and blood vessels.
- These clumps weaken blood vessel lining, disrupt the blood-brain barrier, and impair blood flow.
- New 3D lab models and AI aim to develop treatments targeting both neuronal and vascular damage.
In Parkinson’s disease, toxic clumps of alpha-synuclein protein not only damage brain cells but also weaken the lining of blood vessels, with both processes likely working together to drive disease progression, according to a study by researchers from Binghamton University in New York and Drexel University in Philadelphia.
“Parkinson’s is a multifaceted disease,” Jungwook “Jay” Paek, PhD, an assistant professor in Binghamton University’s department of electrical and computer engineering, said in a Binghamton University press release. “Understanding the complex interplay between neurodegeneration and vascular pathology [disease-causing mechanisms] offers unique opportunities to help patients.”
The study, “Microengineering of the capillary interface of midbrain dopaminergic neurons to study Parkinson’s disease vascular alterations,” was published in Communications Engineering.
New findings shed light on vascular complications
Parkinson’s disease causes the loss of dopaminergic neurons, the nerve cells in the brain that produce dopamine, a chemical needed for motor control. Research has long focused on this loss of dopaminergic neurons, but there are also problems with brain blood vessels that are less well understood.
One hallmark of Parkinson’s is the buildup of alpha-synuclein. Normally, this protein helps nerve cells function, but in Parkinson’s, it can misfold and clump into toxic aggregates that damage dopaminergic neurons. Now, the researchers found that they can also damage the blood vessels that supply the brain with oxygen and nutrients through the protective layer called the blood–brain barrier.
“Before this research, most studies on Parkinson’s disease have focused on the aggregation of specific proteins and their impacts on neurodegeneration,” Paek said. “However, how the protein aggregation contributes to vascular complications remains largely underexplored, so this is an exciting finding.”
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